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Oxidant stress cell membrane consequences

Several adverse consequences result from exposure of the cell to oxidative stress. Cellular proteins with critical -SH residues and membrane polyunsaturated fatty... [Pg.682]

Fig. 2.8. Factors controlling the production of free radicals in cells and tissues (Rice-Gvans, 1990a). Free radicals may be generated in cells and tissues through increased radical input mediated by the disruption of internal processes or by external influences, or as a consequence of decreased protective capacity. Increased radical input may arise through excessive leukocyte activation, disrupted mitochondrial electron transport or altered arachidonic acid metabolism. Delocalization or redistribution of transition metal ion complexes may also induce oxidative stress, for example, microbleeding in the brain, in the eye, in the rheumatoid joint. In addition, reduced activities or levels of protectant enzymes, destruction or suppressed production of nucleotide coenzymes, reduced levels of antioxidants, abnormal glutathione metabolism, or leakage of antioxidants through damaged membranes, can all contribute to oxidative stress. Fig. 2.8. Factors controlling the production of free radicals in cells and tissues (Rice-Gvans, 1990a). Free radicals may be generated in cells and tissues through increased radical input mediated by the disruption of internal processes or by external influences, or as a consequence of decreased protective capacity. Increased radical input may arise through excessive leukocyte activation, disrupted mitochondrial electron transport or altered arachidonic acid metabolism. Delocalization or redistribution of transition metal ion complexes may also induce oxidative stress, for example, microbleeding in the brain, in the eye, in the rheumatoid joint. In addition, reduced activities or levels of protectant enzymes, destruction or suppressed production of nucleotide coenzymes, reduced levels of antioxidants, abnormal glutathione metabolism, or leakage of antioxidants through damaged membranes, can all contribute to oxidative stress.
Beside the bactericidal function of nanosilver discussed in the literature, there are many factors that can cause the undesirable cytotoxicity effect of nanomaterials. The reason for silver s cytotoxicity should also be found in the formation of ROS, which damage the DNA and RNA of the cells by way of apoptosis. Due to the strong reduction-oxidation function (redox) of precious metals, nAg increase the ROS concentration and induce oxidation stress in the cells, initiating the peroxidation process, which causes a deformation of the cell membrane s structure, the latter s depolarization and the inhibition of the membrane enzymes activity. This leads to the loss in the integrity of the cell membrane and a disorder of the oxidative phosphorylation in mitochondria [6], which in consequence, contributes to cell degradation and leads to numerous diseases and accelerated ageing of the body [7]. [Pg.381]


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